Archive for February, 2012

This post was originally published last year. I’m travelling for a few weeks, so I’m reloading some of my favourite stories from 2011. Normal service will resume when I get back.

The hagfish looks like an easy meal. Its sinuous, eel-like body has no obvious defences, but any predator that moves in for a bite is in for a nasty surprise. The hagfish releases a quick-setting slime that clogs up the predator’s gills, causing it to gag, choke and flee. Scientists have known about this repulsive defence for decades, but Vincent Zintzen has finally filmed it in the wild. His videos also prove that hagfish, generally thought to be scavengers of the abyss, are also active hunters that can drag tiny fish from their burrows.

This post was originally published last year. I’m travelling for a few weeks, so I’m reloading some of my favourite stories from 2011. Normal service will resume when I get back.

Meet the world’s smallest farmer – a “social amoeba” that seeds new land with bacteria, which it then eats. Just as human farmers carry seeds and livestock when they move to new areas, the amoeba can prepare for harsh conditions by bringing a ready food supply with it. It joins ants, termites and humans on the list of creatures that practice agriculture.

This post was originally published last year. I’m travelling for a few weeks, so I’m reloading some of my favourite stories from 2011. Normal service will resume when I get back.Two people are dancing a waltz, and it is not going well. One is tall and the other short; one is graceful, the other flat-footed; and both are stepping to completely different rhythms. The result is chaos, and the dance falls apart. Their situation mirrors a problem faced by all complex life on Earth. Whether we’re animal or plant, fungus or alga, we all need two very different partners to dance in step with one another. A mismatch can be disastrous.

Virtually all complex cells – better known as eukaryotes – have at least two separate genomes. The main one sits in the central nucleus. There’s also a smaller one in tiny bean-shaped structures called mitochondria, little batteries that provide the cell with energy. Both sets of genes must work together. Neither functions properly without the other.

Mitochondria came from a free-living bacterium that was engulfed by a larger cell a few billion years ago. The two eventually became one. Their fateful partnership revolutionised life on this planet, giving it a surge of power that allowed it to become complex and big (see here for the full story). But the alliance between mitochondria and their host cells is a delicate one.

Both genomes evolve in very different ways. Mitochondrial genes are only passed down from mother to child, whereas the nuclear genome is a fusion of both mum’s and dad’s genes. This means that mitochondria genes evolve much faster than nuclear ones – around 10 to 30 times faster in animals and up to a hundred thousand times faster in some fungi. These dance partners are naturally drawn to different rhythms.

This is a big and underappreciated problem because the nuclear and mitochondrial genomes cannot afford to clash. In a new paper, Nick Lane, a biochemist at University College London, argues that some of the most fundamental aspects of eukaryotic life are driven by the need to keep these two genomes dancing in time. The pressure to maintain this “mitonuclear match” influences why species stay separate, why we typically have two sexes, how many offspring we produce, and how we age.

This post was originally published last year. I’m travelling for a few weeks, so I’m reloading some of my favourite stories from 2011. Normal service will resume when I get back.

It couldn’t be easier to make sweeping edits on a computer document. If I were so inclined, I could find every instance of the word “genome” in this article and replace it with the word “cake”. Now, a team of scientists from Harvard Medical School and MIT have found a way to do similar trick with DNA. Geneticists have long been able to edit individual genes, but this group has developed a way of rewriting DNA en masse, turning the entire genome of a bacterium into an “editable and evolvable template”.

Their success was possible because the same genetic code underlies all life. The code is written in the four letters (nucleotides) that chain together to form DNA: A, C, G and T. Every set of three letters (or ‘codon’) corresponds to a different amino acid, the building blocks of proteins. For example, GCA codes for alanine; TGT means cysteine. The chain of letters is translated into a chain of amino acids until you get to a ‘stop codon’. These special triplets act as full stops that indicate when a protein is finished.

This code is virtually the same in every gene on the planet. In every human, tree and bacterium, the same codons correspond to the same amino acids, with only minor variations. The code also includes a lot of redundancy. Four DNA letters can be arranged into 64 possible triplets, which are assigned to only 20 amino acids and one stop codon. So for example, GCT, GCA, GCC and GCG all code for alanine. And these surplus codons provide enough wiggle room for geneticists to play around with.

Farren Isaacs, Peter Carr and Harris Wang have started to replace every instance of TAG with TAA in the genome of the common gut bacterium Escherichia coli. Both are stop codons, so there’s no noticeable difference to the bacterium – it’s like replacing every word in a document with a synonym. But to the team, the genome-wide swap will eventually free up one of the 64 triplets in the genetic code. And that opens up many possible applications.

New Scientist had a great new feature on nine lost treasures that science wants back. I wrote about one of them – the bones of Peking Man.

In September 1941, Hu Chengzhi placed several skulls into two wooden crates. Around him, China was at war with Japan, so he was sending the skulls to the US for safekeeping. They never arrived. Hu was among the last people to see one of the most important palaeontological finds in history. These lost skulls belonged to Homo erectus pekinensis, known as Peking Man.

This post was originally published last year. I’m travelling for a few weeks, so I’m reloading some of my favourite stories from 2011. Normal service will resume when I get back.Over the last three years, a group of scientists have been going round two suburbs of Cairns, Australia, and asking local people if they could release mosquitoes on their properties. Ninety percent said yes. These were no ordinary mosquitoes. They had been loaded with bacteria that stop them from passing on the virus that causes dengue fever.

Dengue fever affects thousands of Queenslanders every year. It is caused by an alliance of two parasites – the dengue virus, and the Aedes aegypti mosquito that spreads it. In an ambitious plan to break this partnership, Scott O’Neill from the University of Queensland turned to yet another parasite – a bacterium called Wolbachia. It infects a wide variety of insects and other arthropods, making it possibly the most successful parasite of all. And it has a habit of spreading with great speed.

Wolbachia is transmitted in the eggs of infected females, so it has evolved many strategies for reaching new hosts by screwing over dead-end males. Sometimes it kills them. Sometimes it turns them into females. It also uses a subtler trick called “cytoplasmic incompatibility“, where uninfected females cannot mate successfully with infected males. This means that infected females, who can mate with whomever they like, enjoy a big advantage over uninfected females, who are more restricted. They lay more eggs, which carry more Wolbachia. Once the bacterium gets a foothold in a population, it tends to spread very quickly.

This post was originally published last year. I’m travelling for a few weeks, so I’m reloading some of my favourite stories from 2011. Normal service will resume when I get back.

If you walk by a European river on a summer’s day, you might get to hear the animal kingdom’s champion vocalist. His song sounds like a train of chirps, and from a metre away, it’s as loud as whirring power tools. The din is all the more incredible because it is produced by an insect just two millimetres in length – the lesser water boatman, Micronecta scholtzi

Micronecta means “small swimmer” and it is aptly named. It’s among the smallest of the several hundred species of water boatmen that row across the bottom of ponds and streams with paddle-shaped legs. The males are the ones that sing, and they often do so in large choruses to attract the silent females. These songs are famously loud. Even though the insect lives underwater, you can hear its call from the riverbank, several metres away.

Now, Jérôme Sueur from the Natural History Museum in Paris has measured Micronecta’s song using underwater microphones. He found that it the small swimmer is a record-breaker. On average, it reaches 79 decibels, about the level of a ringing phone or a cocktail party. But at its peak, it reaches 105 decibels – more like a car horn, a power tool or a passing subway train.

This post was originally published last year. I’m travelling for a few weeks, so I’m reloading some of my favourite stories from 2011. Normal service will resume when I get back.

The wing of a fruit fly, viewed against a white background, looks very ordinary. It is transparent, with no obvious colours except for some small brownish spots. But looks can be deceptive. If you put the wing in front of a black background, it suddenly explodes in a kaleidoscope of colour. Oranges, blues, greens, violets – virtually the entire rainbow dances across the wing, except for red.

A French scientist called Claude Charles Goureau first noticed these vivid hues back in 1843. Since then, they have languished in obscurity, “apparently unnoticed by contemporary biologists”. Whenever new species of wasps or flies are described, their discoverers almost never mention the coloured patterns of the wings. The visible pigments have even been described as “evolution in black and white”. It’s like walking through an art gallery with a blindfold.

Now, Ekaterina Shevtsova from Lund University has taken off the blind. By photographing several species against dark backgrounds, she has revealed a world of hidden colour, rivalling that of more obviously beautiful insects. “The claim that fly and wasp wing patterns are no match for the incredible diversity of colourful butterfly wing patterns is obsolete,” she says.

Rant: I really hate it when people in science communication embrace sloppy evidence for some imagined problems with science. For example, this new report makes a big thing of the fact that 83% of UK 10-year-olds say a science career is ‘not for me’. Great! If the 17% who are interested in a science career actually try for one, there’s going to be a lot of unemployed people. I mean, look at Fig 1! That is BRILLIANT. And yet we get a boring science-in-trouble narrative.

Cancer drugs can destabilise mouse genomes for generations. Lead researcher “cautions against extrapolating results… to humans.” Note the responsible reporting: the fact that this is in mice is mentioned in the hed, sub-hed, and first three paragraphs.

I’ve written a few guest posts for the Faculty of 1000’s Naturally Selected blog, covering some interesting papers from last year that I missed here. There’s one about how eggs greet sperm, and another on how sleeping alone affects newborn babies. But the third post is one that I particularly want to draw attention to – it’s about a cancer paper that didn’t get much notice last year, but seems to deserve it. Here’s the first bit:

Tumours are bundles of cells that grow and divide uncontrollably, and their genes are deployed in unusual ways. By analysing the genes from different tumour samples, scientists have tried to pin down the chaotic events that lead to cancer. They seem to be making headway. Dozens of papers have reported “gene expression signatures” that predict the risk of dying or surviving from cancer, and new ones come out every month.

These signatures purportedly hint at how healthy cells transform into tumours in the first place. If, for example, the genes in question are involved in wound healing, this tells you that the healing process is somehow involved in a tumour’s progression. These collections of genes reveal deeper truths about the disease they’re associated with.

This idea sounds reasonable, but David Venet from the Université Libre de Bruxelles has thrown a big spanner into the works. He has shown that completely random sets of genes can predict the odds of surviving breast cancer better than published signatures.

Venet found three signatures that are completely unconnected to cancer. Instead, these collections of genes were associated with laughing at jokes after lunch, with the experience of social defeat in mice, and with the positioning of skin cells. All of them were associated with breast cancer outcomes.

Head over to Naturally Selected for the rest, including how long it took to get this study published.